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Abstract
RpoS, a general stress response regulator, and trehalose had been implicated in helping the cells survive times of stress. Previous study had shown that when the cells were subjected to heat shock, they developed a more tetracycline-resistant state in a phenomenon known as cross-protection. While a role of RpoS has been suggested in the heat-induced cross-protection against tetracycline, the identity of the downstream effector(s) directly responsible for the phenomenon were not elucidated. We investigated if trehalose played a role in conferring tetracycline resistance and if ots A, one of the genes responsible for endogenous trehalose synthesis, was regulated by RpoS. Trehalose accumulation was assessed indirectly via ots A gene expression. The wild type, Δ rpo S, and Δ ots A strains were thermally stressed for various lengths of time. The cells were exposed to tetracycline of various concentrations to determine the resistance state of the cells. Expression of rpo S and ots A were quantified via qPCR. All three strains showed an increase in the level of resistance when exposed to heat shock for 20-30 minutes, while no distinct pattern of gene expression was observed. Our data indicates that rpo S and ots A expression may be independent and may not be involved in establishing heat-induced cross-protection against tetracycline.